Patients with head and neck squamous cell carcinoma with advanced cervical metastases (N2, 3) have a poor prognosis. This is because patients with N3 disease are generally considered unresectable due to adhesions between metastatic nodes and surrounding tissue, and the patients with N2, 3 treated with chemoradiotherapy experience a very high rate of distant failure. Our strategy for patients with N2, 3 is to use the thermochemoradiotherapy with retrograde superselective intra-arterial infusion. Retrograde superselective intra-arterial chemotherapy for head and neck cancer has the advantage of delivering a high concentration of the chemotherapeutic agents to the tumor bed, and provides daily concurrent radiotherapy and chemotherapy. The use of hyperthermia has generally been confined to cervical lymph node metastases accessible with a radiofrequency system employing external application, and in combination with synergistic chemoradiotherapy. This review demonstrates that thermochemoradiotherapy using intra-arterial infusion provided good histopathologic effects and locoregional control rates for advanced oral cancer patients with N2, 3 cervical lymph node metastases.

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Heat shock transcription factor 1 (HSF1) has been shown to act as the major regulator of the heat shock transcriptional response, and plays a central role in the cellular functions of cancer cells. Here, to identify the molecular mechanism of the regulation of cancer cell functions by HSF1, comparative gene expression analysis was performed with mock and HSF1-knockdown cells. Silencing of HSF1 in human oral squamous cell carcinoma (OSCC) HSC-3 cells was carried out by siRNA technology. Almost complete knockdown of the expression of HSF1 protein was observed in the cells treated with siRNA for HSF1. Knockdown of HSF1 significantly decreased the number of viable cells and induced cell death. Global gene expression analysis indicated that 31 genes were up-regulated and 98 genes were down-regulated by > 2-fold in HSF1-knockdown cells. We identified gene networks U and D, which were obtained from up- and down-regulated genes, respectively, using Ingenuity Pathways Analysis tools. The gene networks U and D contained genes that were associated with induction and prevention of cell death, respectively. The present results indicate that HSF1-knockdown affects the expression of a large number of genes and provide additional novel insight into the molecular basis of cell death induced by HSF1 in OSCC.

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